HLA Class I Subtype-Dependent Expansion of KIR3DS1(+) and KIR3DL1(+) NK Cells during Acute Human Immunodeficiency Virus Type 1 Infection

Author:

Alter, G.

Rihn, S.

Walter, K.

Nolting, A.

Martin, M.

Rosenberg, E. S.

Miller, J. S.

Carrington, M.

Altfeld, M.
Author Address

Alter, Galit, Rihn, Suzannah, Walter, Katharine, Nolting, Anne, Rosenberg, Eric S.; Altfeld, Marcus] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Infect Dis Unit, Boston, MA 02129 USA. [Alter, Galit, Rihn, Suzannah, Walter, Katharine, Nolting, Anne, Rosenberg, Eric S.; Altfeld, Marcus] Harvard Univ, Ragon Inst MGH MIT & Harvard, Sch Med, Boston, MA 02129 USA. [Alter, Galit, Rihn, Suzannah, Walter, Katharine, Nolting, Anne, Rosenberg, Eric S.; Altfeld, Marcus] Harvard Univ, Div AIDS, Sch Med, Boston, MA 02129 USA. [Martin, Maureen, Carrington, Mary] SAIC Frederick Inc, Basic Res Program, Lab Genom Div, Frederick, MD USA. [Miller, Jeffrey S.] Univ Minnesota, Ctr Canc, Div Hematol Oncol & Transplantat, Minneapolis, MN USA.

Abstract:

NK cells are critical in the early containment of viral infections. Epidemiological and functional studies have shown an important role of NK cells expressing specific killer immunoglobulin-like receptors (KIRs) in the control of human immunodeficiency virus type 1 (HIV-1) infection, but little is known about the mechanisms that determine the expansion of these antiviral NK cell populations during acute HIV-1 infection. Here we demonstrate that NK cells expressing the activating receptor KIR3DS1(+) and, to a lesser extent, the inhibitory receptor KIR3DL1(+) specifically expand in acute HIV-1 infection in the presence of HLA-B Bw480I, the putative HLA class I ligand for KIR3DL1/3DS1. These data demonstrate for the first time the HLA class I subtype-dependent expansion of specific KIR+ NK cells during an acute viral infection in humans.

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